Coordinate control of adipose ‘browning’ and energy expenditure by β-adrenergic and natriuretic peptide signalling

Collins, Sheila; Sarzani, Riccardo; Bordicchia, Marica

doi:10.1038/ijosup.2014.6

Cited by 17 publications

(23 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…ANP activity depends on the ratio of ANP receptor NPR1 and clearance receptor NPR3 [29]. Obesity-induced rats fed a high-fat diet have a lower NPR1/NPR3 ratio than the normal diet [30]. In addition, mice knocked out of NPR3 have similar effects to ANP-induced brown fat thermogenic program [31].…”

Section: Discussionmentioning

confidence: 99%

Expression and Secretion of an Atrial Natriuretic Peptide in Beige-Like 3T3-L1 Adipocytes

Bae

Kim

2019

IJMS

View full text Add to dashboard Cite

The browning of white adipose tissue (beige adipocytes) stimulates energy expenditure. Omega-3 fatty acids have been shown to induce thermogenic action in adipocytes via G-protein coupled receptor 120 (GPR120). Atrial natriuretic peptide (ANP) is a peptide hormone that plays the role of maintaining normal blood pressure in kidneys to inhibit Na+ reuptake. Recently, ANP was found to induce adipocyte browning by binding to NPR1, an ANP receptor. However, the expression of ANP in adipocytes has not yet been studied. Therefore, in this study, we investigate the expression of ANP in beige-like adipocytes induced by docosahexaenoic acids (DHA), T3, or a PPAR agonist, rosiglitazone. First, we found that brown adipocyte-specific genes were upregulated in beige-like adipocytes. DHA promoted ANP expression in beige-like cells, whereas DHA-induced ANP expression was abolished by GPR120 knockout. ANP secretion of beige-like adipocytes was increased via PKC/ERK1/2 signaling in the GPR120 pathway. Furthermore, ANP secreted from beige-like adipocytes acted on HEK-293 cells, the recipient cells, leading to increased cGMP activity. After the NPR1 knockdown of HEK-293 cells, cGMP activity was not changed. Taken together, our findings indicate that beige-like adipocytes induce ANP secretion, which may contribute to improving obesity-associated metabolic disease.

show abstract

Section: Discussionmentioning

confidence: 99%

Expression and Secretion of an Atrial Natriuretic Peptide in Beige-Like 3T3-L1 Adipocytes

Bae

Kim

2019

IJMS

View full text Add to dashboard Cite

show abstract

“…However, more recently it is appreciated that cGMP-regulated pathways have similar effects in adipose tissue (reviewed in [27] , [28] ). We previously showed that ANP and BNP, which increase intracellular cGMP and PKG activity through their membrane-bound guanylyl cyclase-coupled receptor NPRA, comprise a signaling pathway in adipocytes that parallels that of the SNS and βARs [1] , [29] . Given that the cyclic nucleotides cAMP and cGMP lead to PKA and PKG phosphorylation of closely conserved amino acid motifs [30] , we asked whether mTORC1 was also essential for cGMP-PKG evoked induction of thermogenic adipocytes.…”

Section: Discussionmentioning

confidence: 99%

Cardiac natriuretic peptides promote adipose ‘browning’ through mTOR complex-1

Liu

Ceddia

Collins

2018

Molecular Metabolism

View full text Add to dashboard Cite

ObjectiveActivation of thermogenesis in brown adipose tissue (BAT) and the ability to increase uncoupling protein 1 (UCP1) levels and mitochondrial biogenesis in white fat (termed ‘browning’), has great therapeutic potential to treat obesity and its comorbidities because of the net increase in energy expenditure. β-adrenergic-cAMP-PKA signaling has long been known to regulate these processes. Recently PKA-dependent activation of mammalian target of rapamycin complex 1 (mTORC1) was shown to be necessary for adipose ‘browning’ as well as proper development of the interscapular BAT. In addition to cAMP-PKA signaling pathways, cGMP-PKG signaling also promotes this browning process; however, it is unclear whether or not mTORC1 is also necessary for cGMP-PKG induced browning.MethodActivation of mTORC1 by natriuretic peptides (NP), which bind to and activate the membrane-bound guanylyl cyclase, NP receptor A (NPRA), was assessed in mouse and human adipocytes in vitro and mouse adipose tissue in vivo.ResultsActivation of mTORC1 by NP-cGMP signaling was observed in both mouse and human adipocytes. We show that NP-NPRA-PKG signaling activate mTORC1 by direct PKG phosphorylation of Raptor at Serine 791. Administration of B-type natriuretic peptide (BNP) to mice induced Ucp1 expression in inguinal adipose tissue in vivo, which was completely blocked by the mTORC1 inhibitor rapamycin.ConclusionOur results demonstrate that NP-cGMP signaling activates mTORC1 via PKG, which is a component in the mechanism of adipose browning.

show abstract

“…This study showed that expression of PPKA was higher significantly in the HFZ group. β-AR, members of the G protein-coupled receptors play important roles in the regulation of metabolism function [34][35][36]. Previous research reported that ZAG may exert function by associating with β2-AR and β3-AR in white adipose tissue [37][38][39].…”

Section: Discussionmentioning

confidence: 99%

Effects of Zinc Alpha2 Glycoprotein on Lipid Metabolism of Liver in High-Fat Diet-Induced Obese Mice

et al. 2017

View full text Add to dashboard Cite

Zinc alpha2 glycoprotein (ZAG) is a new type of adipokine involved in adipose tissue mobilization, however, little is known about its lipid metabolism effect in liver. Therefore, we investigated the effects of ZAG in the regulation of hepatic lipid accumulation. Mice were randomly divided into two groups; one was fed a normal diet and another was fed a high-fat diet for eight weeks to establish obesity model. After that, the normal diet group was divided into ND (injection of pcDNA3.1) and NDZ (injection of ZAG recombinant plasmid) and the high-fat diet group was divided into HF (injection of pcDNA3.1) and HFZ (injection of ZAG recombinant plasmid). The mice were weighed once per week and injected with plasmid once every three days for eight times. The results showed that body weight and hepatic TG content were decreased dramatically in HFZ group compared with HF group. The stearoyl-CoAdesaturase1 (SCD1) and Acyl-CoA Synthetase-1 (ACSS1) protein levels in HFZ group were significantly decreased. Furthermore, phosphorylated hormone sensitive lipase (P-HSL) was significantly higher in HFZ group. In HFZ group, hepatic fatty acid translocase (CD36) and fatty acids binding protein-1 (FABP1) protein levels were reduced. In addition, the expression of phosphorylated protein kinase A (PPKA) in HFZ group was higher than the HF group. Meanwhile, NDZ group showed significantly decreased body weight and increased P-HSL level though the hepatic TG content showed no significantly changes compared with the ND group. Therefore, we conclude that ZAG may be beneficial for preventing high-fat-diet-induced hepatic lipid metabolic disorders.

show abstract

Coordinate control of adipose ‘browning’ and energy expenditure by β-adrenergic and natriuretic peptide signalling

Cited by 17 publications

References 39 publications

Expression and Secretion of an Atrial Natriuretic Peptide in Beige-Like 3T3-L1 Adipocytes

Expression and Secretion of an Atrial Natriuretic Peptide in Beige-Like 3T3-L1 Adipocytes

Cardiac natriuretic peptides promote adipose ‘browning’ through mTOR complex-1

Effects of Zinc Alpha2 Glycoprotein on Lipid Metabolism of Liver in High-Fat Diet-Induced Obese Mice

Contact Info

Product

Resources

About